These drugs act primarily on the peripheral
vasculature and reduce the workload on the heart. Some vasodilators, e.g. nitrates,
cause venodilation, reducing venous return to the heart, and thereby decreasing systemic
and pulmonary venous pressures (preload). Others, e.g. hydralazine, cause arteriodilation
thus reducing afterload on the left ventricle. Some vasodilators, e.g. prazosin,
nitroprusside and the angiotensin-converting enzyme (ACE) inhibitors (e.g. enalapril
and captopril) have effects on preload and afterload.
Conventional vasodilators such as hydralazine and isosorbide dinitrate stimulate
the sympathetic system and the renin-angiotensin-aldosteron-ADH system resulting
in sodium and water retention, which may be detrimental to some patients. Therefore they are
probably best used in combination with cardiac glycosides and diuretics.
Concurrent treatment with ACE inhibitors (e.g. enalapril) offers a good therapeutic
approach to clinical cases not responding to diuretics and digoxin therapy alone.
Marked hypotension can be a problem following the initial oral dose of an ACE inhibitor
particularly in patients on diuretics or on a low salt diet, and patients are best
hospitalised during the introduction of ACE inhibitors. Any drug that induces hypotension
may precipitate prerenal azotaemia and acute renal failure in at-risk patients, and ACE inhibitors
are contraindicated in the presence of renal impairment. In old animals renal function
should be monitored closely before, and for at least a week after the use of these
drugs, and diuretic doses should be reduced when they are administered at the same